Notes

Potassium Homeostasis:
Potassium is able to be secreted. Potassium is attracted to negatively charged proteins within the cell. Concentration is partly maintained by Na+/K+ ATPase pump.
Dependent on: food intake, plasma osmolality, metabolic acidosis, and cell lysis.
Kidneys maintain K+ balance by regulating movement between ICF and ECF, but this can take a while so initially K+ increase during meals is maintained by movement of potassium in and out of the skeletal muscles to prevent hyperkalemia. This is achieved by stimulation of these cells from epinephrine, aldosterone, and insulin, which triggers K+ uptake into the cells via ATPase and symporters.
Regulation of K+ secretion depends on alterations in K+ secretions by principal and intercalated cells
Potassium transport in PT:
ATPase pump keeps Na+ low. Primary reabsorption occurs paracellular due to solvent drag, but also due to luminal voltage becoming more positive. K+ channels on apical surface and basolateral surface push K+ out.
Potassium transport in TAL:
K+ channels on apical surface move K+ out, NKCC2 transporters bring potassium in. Apical channels also generate a positive lumen voltage that pushes K+ ions paracellularly.
Potassium transport in early and late DCT:
DCT1(early): K+ channels on basolateral and apical surface + K+Cl- symporter on apical side. ATPase pump brings potassium into the cells.
DCT2(late): electrogenic transport mediated by epithelial Na+ transporters, K+ chnnaels, and aldosterone sensitivity.
Potassium transport in Collecting Duct:
Principal cells secrete K+ due to high expression of ATPase pumps on basolateral side and K+ channels on apical side. Intercalated cells reabsorb K+ via H+/K+ ATPase on basolateral side. H+ antiporter also moves hydrogen out of the cell. H+ comes from cellular metabolism. HCO3-/Cl- antiporter brings chloride into cells. Cl- and K+ channels on basolateral surface for reabsorption.
Factors that influence K+ Secretion: Increased Plasma K+ conc., Aldosterone, ADH
-Plasma: increased Na+/K+ expression --> increased K+ secretion, increased permeability of apical membrane to K+, increased tubular flow rate
-Aldosterone: Aldosterone binds to mineralcorticoid receptor inside the cell and translocates to the nucleus increasing K+ secretion
-ADH: No net effect because ADH causes increased ENaC channels and reduces tubular flow rate, which oppose each other.
Tubular flowrate increases K+ secretion because bending of cilia activates calcium transporters, calcium can activate K+ channels